Recent studies have shown that aortic blood flow during cardiopulmonary resuscitation (CPR) is due to the generalized increase in pleural pressure rather than direct compression of the heart. It appears that during CPR, blood is expressed primarily from the pulmonary circulation with the ventricles acting as passive conduits. We developed a mathematical model for CPR blood flow by this mechanism. We propose to test this mathematical model in an isolated heart-lung within a pressurized box to determine if this is a plausible mechanism of CPR blood flow. We propose to study the effects of magnitude, frequency, and duration of pleural pressure oscillation on blood flow in the isolated organ model, and to determine if this is consistent with the proposed theoretical mode. In this same system, we will investigate the efficiency of CPR in sustaining total and regional coronary blood flow, and the effects of negative pleural pressures during CPR on coconary perfusion. Finally, the results of these studies will be applied in studies with intact canine preparations. If adequate cardiac output and coronary blood flow can be maintained, then it may be possible to support the circulation for prolonged periods with the non-beating heart using pleural pressure oscillations.